Stem Cell Therapy Genetics and Rheumatoid Arthritis
What do genes have to do with arthritis? No. not those kinds of genes. these kinds of jeans. Genetics can explain why infections can trigger rheumatoid arthritis Appearing in Science Codex was an article describing a new international study that has revealed how genetics could explain why different environmental exposures can trigger the onset of different forms of rheumatoid arthritis. A team at the Arthritis Research UK Centre for Genetics and Genomics at The University of Manchester published their findings in the American Journal of Human Genetics. A proportion of rheumatoid arthritis patients.
Test positive for autoantibodies, while 30% remain seronegative. In this study, the researchers have better defined the genetic distinction between these two disease subtypes: seropositive and seronegative rheumatoid arthritis. They have now established that different genetic variants of a protein that plays a vital role in how the body’s immune system fights infection are associated with the two forms of rheumatoid arthritis. This provides clues to the theory that exposure to different infectious agents, such as bacteria or viruses, trigger the different forms of rheumatoid arthritis in susceptible individuals. Steve Eyre from the genetics and genomics centre in Manchester commented: quot;We recognise.
That rheumatoid arthritis is a complex disease that can have variable presentation and outcomes for different people, in particular in the way they respond to treatment. These findings add to our ability to genetically define subtypes of rheumatoid arthritis, which is an important step towards selecting the best treatment for each patient.quot; Comment: Seropositive and sero negative rheumatoid arthritis behave differently and this is an exciting discovery.
Genetic Risk Factor for Rheumatoid Arthritis and Lupus
Genetic Risk. A longtime collaborative research program has identified a genetic variation that increases the risk of two autoimmune diseases: rheumatoid arthritis, or RA, and systemic lupus erythematosus, or lupus.
Elaine Remmers and her colleagues used a large number of DNA samples from people with RA, lupus, or neither disease. They tested variants within 13 specific genes located in a region of chromosome 2 associated with RA to see if these genetic variations appeared in any of the samples. Among the variants they examined, the researchers found several genetic differences in a gene, known as STAT4.
STAT4 is important because it encodes a protein that plays a role in the regulation and activation of certain cells of the immune system. The investigators learned that one variant form of the gene was present much more often in samples from RA patients compared with people without RA. The scientists replicated that result in two independent collections of.
RA cases and controls. The researchers also found that the same variant of the STAT4 gene was even more strongly linked with lupus in three independent collections from patients and people without lupus. The results suggest that people who carry two copies of the form of the STAT4 gene associated with disease have a 60percent increased risk for RA and more than double the risk for lupus compared with people who carry no copies of that form of the gene.
The research also suggests a shared disease pathway for RA and lupus. The success of the study can be attributed in part to the productive, longstanding collaboration between NIAMS intramural researchers and other scientists that the Institute supports around the country. For more information, please visit our Web site at niams.nih.gov.